RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Postoperative Natural Killer Cell Dysfunction: The Prime Suspect in the Case of Metastasis Following Curative Cancer Surgery.
Postoperative Natural Killer Cell Dysfunction: The Prime Suspect in the Case of Metastasis Following Curative Cancer Surgery.
分数与星级只用于站内排序 —— 不代表疗效、安全性或个人适用性。
手术切除是实体瘤根治治疗的基础,但由于难以清除微转移灶,术后转移复发仍令人担忧。矛盾的是,尽管切除原发肿瘤有益,手术创伤造成的生理应激却可能促进癌症复发和转移。术后环境会抑制重要的抗肿瘤免疫效应细胞,包括自然杀伤(NK)细胞。文献提示,NK细胞是手术后即刻形成转移灶的重要调节者。本综述将介绍手术后直接或间接诱导NK细胞受抑、从而促进微转移灶形成的机制,包括组织缺氧、神经内分泌激活、高凝状态、促炎阶段和抗炎阶段。本文还将考察围手术期治疗策略预防或逆转NK细胞功能障碍的潜力,以期通过阻止手术诱发的转移改善癌症结局。
Surgical resection is the foundation for the curative treatment of solid tumors.
However, metastatic recurrence due to the difficulty in eradicating micrometastases remain a feared outcome. Paradoxically, despite the beneficial effects of surgical removal of the primary tumor, the physiological stress resulting from surgical trauma serves to promote cancer recurrence and metastasis. The postoperative environment suppresses critical anti-tumor immune effector cells, including Natural Killer (NK) cells. The literature suggests that NK cells are critical mediators in the formation of metastases immediately following surgery.
The following review will highlight the mechanisms that promote the formation of micrometastases by directly or indirectly inducing NK cell suppression following surgery. These include tissue hypoxia, neuroendocrine activation, hypercoagulation, the pro-inflammatory phase, and the anti-inflammatory phase. Perioperative therapeutic strategies designed to prevent or reverse NK cell dysfunction will also be examined for their potential to improve cancer outcomes by preventing surgery-induced metastases.
在 PubMed 查看 → 出版商原文(DOI) 全文 PDF(PMC)· 可下载 治疗专题与资料阅读指南 资料来源与翻译说明 报告译文或资料问题 →
MEMBER ACCOUNT
登录成功会直接打开下一页。